We propose to investigate mechanisms accountable for hyperserotonemia (a significant increase in blood levels of serotonin) found in autistic and/or severely retarded children and in other psychiatric and neurological patient populations as a step toward understanding the clinical significance of this phenomenon. We will investigate (1) peripheral blood measures of tryptophan metabolism and (2) possible platelet abnormalities oncomitant measures of blood and urinary tryptophan metabolitse steady-state and following a tryptophan load. Platelet paramenters that will be investigated include platelet number, MAO, uptake, binding and efflux. Because of platelet heterogeneity, we will investigate in a selected group of hyperserotonemic individuals (and those with normal blood levels of serotonin), these various platelet parameters in (1) total platelet populations (2) platelet fractions separated according to density. Since hyperserotonemia may arise as a consequence of different mechanisms in diferent patient populations, these mechanisms will be investigated according to diagnostic criteria. These studies will hope to elucidate the importance of state versus trait variables and will separate those abnormalities in tryptophan metabolsim related to mechanisms of hyperserotonemia from abnormalities related to diagnosis. A better understanding of mechanisms may serve to guide therapeutic intervention.